| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Research Abstract |
Acetylcholine (ACh, 10 μM) stimulation caused cell shrinkage and activation of exocytotic events mediated via intracellular Ca^<2+> concentration ([Ca^<2+>]i) in antral mucus cells of guinea pig, and ACh- evoked exocytosis was modulated by cell shrinkage. Application of a hyposmotic stress, infusion of Cl^--free solution and addition of bumetanide, which caused reduction of [Cl^-]i, potentiated ACh- evoked exocytotic events. These indicate that decreases in [Cl^-]i appears to potentiate ACh-evoked exocytotic events. Isolated antral mucus cells were treated with nystatin to alter [Cl^-]i. As [Cl^-li increase from 5 to 155.5 mM, the frequency of ACh-evoked exocytotic events declines approximately 50%. Thus, reduction of [Cl-]i potentiated ACh-evoked exocytotic events. Treatment with pertussis toxin (PTX), which inhibits G proteins, eliminated the [Cl^-]i dependency of ACh-evoked exocytosis. The Ca^<2+>-regulated exocytosis was modulated by G proteins, which are PTX-sensitive and inhibited by intracellular Cl^-.
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